Considering the pro-inflammatory role of Th1 and Th17 cells and the anti-inflammatory role of Treg cells in MS pathogenesis, and our findings that FOXP3-EXOs regulated Th/Treg immune homeostasis in vitro and in vivo, we suggest that the suppression of EAE development by FOXP3-EXOs may be related to its reversion of Th/Treg immune imbalance. Here, FOXP3 is linked to myeloid sarcoma.